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pubmed-2187482
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| recordtype |
oai_dc
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pubmed-21874822008-04-17 Gene conversion between murine class II major histocompatibility complex loci. Functional and molecular evidence from the bm 12 mutant Articles The experiments presented in this study define the molecular basis of the bm 12 mutation. Initial characterization of an alloreactive T cell clone, 4.1.4, showed this clone to recognize an allodeterminant present on the E beta b and A beta bm12 chains, but not on the bm 12 parent A beta b chain. To define the extent of sequence shared between the I-E beta product and the mutant I-A beta product, we isolated a cDNA clone of the E beta b gene and determined its nucleotide sequence. Comparison of the nucleotide sequences of E beta b, A beta b, and A beta bm12 shows the the A beta bm12 gene to be identical to the E beta b gene in the region where it differs from its A beta b parent. We predict that the bm 12 mutation arose by gene conversion of this region, which spans 14 nucleotides between amino acid residues 67-71 of the mature A beta chain, from the E beta b locus to the corresponding position at the A beta b locus. Recognition of this region, which spans one of the previously defined E beta allelic "hypervariable" regions, by an alloreactive T cell clone provides the first direct evidence of the functional importance of these hypervariable regions in T cell stimulation. The identification of a gene conversion event involving one of these allelic variable regions implicates conversion as a mechanism that acts on class II beta genes to create sequence diversity in regions of Ia molecules that interact with foreign antigen or a T cell receptor, regions where protein sequence polymorphism would presumably be selected for by the expanded ability it affords the organism to mount effective immune responses against a wider variety of foreign antigens. The Rockefeller University Press 1984-10-01 /pmc/articles/PMC2187482/ /pubmed/6434690 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
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| repository_type |
Open Access Journal
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| institution_category |
Foreign Institution
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| institution |
US National Center for Biotechnology Information
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| building |
NCBI PubMed
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| collection |
Online Access
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| language |
English
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| format |
Online
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| title |
Gene conversion between murine class II major histocompatibility complex loci. Functional and molecular evidence from the bm 12 mutant
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| spellingShingle |
Gene conversion between murine class II major histocompatibility complex loci. Functional and molecular evidence from the bm 12 mutant
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| title_short |
Gene conversion between murine class II major histocompatibility complex loci. Functional and molecular evidence from the bm 12 mutant
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| title_full |
Gene conversion between murine class II major histocompatibility complex loci. Functional and molecular evidence from the bm 12 mutant
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| title_fullStr |
Gene conversion between murine class II major histocompatibility complex loci. Functional and molecular evidence from the bm 12 mutant
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| title_full_unstemmed |
Gene conversion between murine class II major histocompatibility complex loci. Functional and molecular evidence from the bm 12 mutant
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| title_sort |
gene conversion between murine class ii major histocompatibility complex loci. functional and molecular evidence from the bm 12 mutant
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| description |
The experiments presented in this study define the molecular basis of the bm 12 mutation. Initial characterization of an alloreactive T cell clone, 4.1.4, showed this clone to recognize an allodeterminant present on the E beta b and A beta bm12 chains, but not on the bm 12 parent A beta b chain. To define the extent of sequence shared between the I-E beta product and the mutant I-A beta product, we isolated a cDNA clone of the E beta b gene and determined its nucleotide sequence. Comparison of the nucleotide sequences of E beta b, A beta b, and A beta bm12 shows the the A beta bm12 gene to be identical to the E beta b gene in the region where it differs from its A beta b parent. We predict that the bm 12 mutation arose by gene conversion of this region, which spans 14 nucleotides between amino acid residues 67-71 of the mature A beta chain, from the E beta b locus to the corresponding position at the A beta b locus. Recognition of this region, which spans one of the previously defined E beta allelic "hypervariable" regions, by an alloreactive T cell clone provides the first direct evidence of the functional importance of these hypervariable regions in T cell stimulation. The identification of a gene conversion event involving one of these allelic variable regions implicates conversion as a mechanism that acts on class II beta genes to create sequence diversity in regions of Ia molecules that interact with foreign antigen or a T cell receptor, regions where protein sequence polymorphism would presumably be selected for by the expanded ability it affords the organism to mount effective immune responses against a wider variety of foreign antigens.
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| publisher |
The Rockefeller University Press
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| publishDate |
1984
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| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2187482/
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| _version_ |
1611427760730800128
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